ORIGINAL ARTICLE Cardiovascular Disorders
http://dx.doi.org/10.3346/jkms.2014.29.5.685 • J Korean Med Sci 2014; 29: 685-690
The Relationship Between J Wave on the Surface Electrocardiography and Ventricular Fibrillation during Acute Myocardial Infarction Soo-Han Kim, Dae-Hyeok Kim, Sang-Don Park, Yong-Soo Baek, Seong-Ill Woo, Sung-Hee Shin, Jun Kwan, and Keum-Soo Park Department of Internal Medicine, Inha University Hospital, Incheon, Korea Received: 4 September 2013 Accepted: 20 March 2014 Address for Correspondence: Dae-Hyeok Kim, MD Department of Internal Medicine, Inha University Hospital, 27 Inhang-ro, Jung-gu, Incheon 400-711, Korea Tel: +82.32-890-2440, Fax: +82.32-890-2447 E-mail: [email protected]
We investigated whether the presence of J wave on the surface electrocardiography (sECG) could be a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (AMI). We performed a retrospective study of 317 patients diagnosed with AMI in a single center from 2009 to 2012. Among the enrolled 296 patients, 22 (13.5%) patients were selected as a VF group. The J wave on the sECG was defined as a J point elevation manifested through QRS notching or slurring at least 1 mm above the baseline in at least two leads. We found that the incidence of J wave on the sECG was significantly higher in the VF group. We also confirmed that several conventional risk factors of VF were significantly related to VF during AMI; time delays from the onset of chest pain, blood concentrations of creatine phosphokinase and incidence of ST-segment elevation. Multiple logistic regression analysis demonstrated that the presence of J wave and the presence of a ST-segment elevation were independent predictors of VF during AMI. This study demonstrated that the presence of J wave on the sECG is significantly related to VF during AMI. Keywords: J Wave; Ventricular Fibrillation; Acute Myocardial Infarction
INTRODUCTION
MATERIALS AND METHODS
Primary ventricular fibrillation (PVF) during acute myocardial infarction (AMI) refers to VF that occurs early (usually < 48 hr post myocardial infarction), and is not associated with recurrent ischemia or heart failure (1). The incidence of VF was reported to be more than 10% during AMI, and VF usually occurs in a few hours after the onset of chest pain (1). VF is the most frequent cause of death in association with AMI because it usually occurs before medical contact (1). Recent studies have demonstrated that J wave on the sECG has been associated with idiopathic VF in patients who do not have structural heart disease (2). A recent study also reported that the presence of J wave is associated with ventricular arrhythmia in patients who have chronic coronary artery disease (3). So far, few studies reported that the presence of J wave in sECG is associated with VF during AMI (1, 4-6). Several variables, including J wave, were reported as significant predictors of VF, but failed to get statistical significance. Through this study, we planned to evaluate that the presence of J wave on the sECG could be a potential risk factor for VF during AMI.
Patient selection and data collection We performed a retrospective study of 317 patients diagnosed with AMI in a single center from 2009 to 2012. Among the involved 317 patients, especially in the VF group, 21 patients who did not have a sECG before AMI were excluded in this group. As a result, 22 patients were selected as the VF group and 296 patients were enrolled for data analysis. Finally, all patients were classified as having a VF or not (VF group: n = 22 [13.5%], the non-VF group : n = 274 [86.5%]). Furthermore, all patients selected for this study received coronary angiography and underwent percutaneous coronary interventions (PCIs). We perform ed a subgroup analysis according to the location of the infarction, and the infarct-related artery (IRA) were left anterior descending (LAD) artery (45.4%), left circumflex (LCX) artery (6.1%), right coronary artery (RCA) (48.5%), diagonal branch (0.3%) and left main artery (1.0%), respectively. We also checked a pre-PCI Thrombolysis In Myocardial Infarction (TIMI) flow grade before the coronary intervention.
© 2014 The Korean Academy of Medical Sciences. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
pISSN 1011-8934 eISSN 1598-6357
Kim S-H, et al. • Relationship between J Wave and Ventricular Fibrillation ECG analysis The latest ECG before AMI was reviewed for J wave characteristics. Twelve-lead ECGs were digitally downloaded from the GE Marquette MUSE system (GE Medical Systems, Milwaukee, WI, USA) and were also analyzed digitally (Adobe Acrobat X Professional; Adobe Systems Incorporated, San Jose, CA, USA). Three investigators performed ECG analysis separately and randomly to confirm correct J wave patterns. The early repolarization on the sECG was defined as J point elevations manifested through QRS notching or slurring for at least 1 mm (0.1 mV) above the baseline in at least two consecutive inferior or lateral leads. As defined through prior studies, QRS notching in ECG was defined as a positive deflection at the terminal portion of a positive QRS complex. QRS slurring in ECG was defined as a smooth transition from the QRS complex to the ST segment with upright concavity. We excluded ECGs of Brugada pattern which have J wave in anterior precordial leads (V1-V3). We measured the amplitude of J wave at the peak of the positive deflection in case of notched pattern and at the QRS-ST junction in slurred pattern. Statistics Statistical analyses were performed with SPSS statistical software (version 12.K; SPSS, Inc., Chicago, IL, USA). Continuous variables were expressed as mean ± SD and were compared by t tests. Categorical variables were expressed as percentages and
were compared by chi-square statistics or Fisher’s exact test as indicated. A multiple logistic regression analysis was used to identify the subset of variables as predictors of VF during AMI. Analyses were considered significant at a P value < 0.05 (2-tailed). Ethics statement The study protocol was reviewed and approved by the institutional review board of Inha University Hospital (Protocol No. 12-103). Informed consents were waived by the institutional review board (IRB).
RESULTS Demographic and clinical characteristics of all AMI patients Table 1 shows baseline characteristics of the study population. Among the total 22 patients of the VF group, 16 patients were males and 6 patients were females. The mean age of the VF group was a 59.95 ± 12.94 yr. The non-VF group consisted of 274 patients and male was also predominant in numbers which were 207. The mean age of the non-VF group was 61.33 ± 13.47 and was not statistically different from that of the VF group (P = 0.644). VF occurred before ER arrival in 9 patients, during ER stay before PCI in 5 patients, during PCI in 1 patient, and within 48 hr after PCI in 7 patients. In this study, we excluded patients with VF after 48 hr from the onset of chest pain. The mean time gap
Table 1. Baseline characteristics of patients between the VF group and the non-VF group Parameters
Total (n = 296)
VF group (n = 22)
Non-VF group (n = 274)
P value
Age (yr) Gender (female/male) Cardiac risk factor, No. (%) Smoking Diabetes mellitus Hypertension LDL(mg/dL) Infarct-related artery, No. (%) LAD LCX RCA Diagonal Left main trunk Pre-PCI TIMI 0, No. (%) Coronary artery disease, No. (%) One vessel disease Two vessel disease Three vessel disease Normal vessel Echocardiography LVEF LA diameter Time delay from the onset of chest pain (min) Peak CK level, IU/L ST-segment elevation, No. (%)
61.23 ± 13.41 73/223
59.95 ± 12.94 6/16
61.33 ± 13.47 67/207
0.644 0.798
176 (59.5) 64 (21.6) 155 (52.4) 117.25 ± 34.76
14 (63.6) 2 (9.1) 9 (40.9) 112.30 ± 30.29
162 (59.1) 62 (22.6) 146 (53.3) 117.64 ± 35.11
0.43 0.107 0.185 0.509 0.462
133 (45.4) 47 (6.1) 111 (48.5) 1 (0.3) 3 (1.0) 168 (57.1)
13 (61.9) 1 (4.8) 7 (33.3) 0 (0) 0 (0) 14 (66.7)
120 (43.8) 46 (16.8) 104 (37.9) 1 (0.4) 3 (1.1) 154 (56.4)
148 (50.3) 81 (27.6) 63 (21.4) 2 (0.7)
13 (61.9) 4 (19.0) 3 (14.3) 1 (4.8)
135 (49.5) 77 (28.2) 60 (21.9) 1 (0.4)
46.57 ± 8.48 39.00 ± 5.44 717.6 ± 1759.2 2,654.87 ± 4103 193 (65.2)
49.71 ± 8.37 37.33 ± 4.52 634.6 ± 135.3 12,429.78 ± 2650 21 (95.5)
46.32 ± 8.45 39.14 ± 5.49 1,815.6 ± 109.8 2,285.97 ± 138 172 (62.8)
0.493 0.064
0.078 0.144 0.007 0.001 0.001
LDL, low density lipoprotein; LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery; PCI, percutaneous coronary intervention; TIMI, thrombolysis in myocardial infarction; LVEF, left ventricular ejection fraction; CK, creatine phosphokinase.
686 http://jkms.org
http://dx.doi.org/10.3346/jkms.2014.29.5.685
Kim S-H, et al. • Relationship between J Wave and Ventricular Fibrillation from acquisition of the latest ECGs to occurrence of VF was 266 days in the VF group. In this group, the distributions of time gap were over 1 yr in 5 patients, between 1 month and 1 yr in 13 patients, and within 1 month in 4 patients. There was no statistical difference in the locations of IRA, or TIMI flow before PCI between the two groups. Also, there was no statistical difference in the numbers of stenosed coronary arteries and echocardiographic parameters, including ejection fractions of left ventricle and diameters of left atrium. Cardiac deaths were noted both in the VF group (n = 1, 4.5%) vs in the non-VF group (n = 1, 0.4%), which were not different statistically (P = 0.150). Fig. 1 shows baseline ECGs in AMI patients. Fig. 1A and Fig. 1B show notched J wave (arrows) in inferior (Fig. 1A) and lateral (Fig. 1B) leads in patients who had an event of VF, whereas Fig. 1C and D show no J wave in inferior (Fig. 1C) or lateral (Fig. 1D) leads in patients who showed no VF during AMI.
Predictors of VF during AMI We found that several conventional risk factors of VF were significantly related to VF during AMI; a time delay from the onset of chest pain to the arrival to emergency room (ER) was significantly shorter in the VF group (634.6 ± 135.3 min vs 1,815.6 ± 109.8 min; P = 0.001, Table 1). Patients in the VF group had a larger IRA, in other words, a greater cardiac enzyme level. Hence, blood concentration of creatine phosphokinase (CK) was significantly higher in the VF group (12,429.78 ± 2,650 IU/L vs 2,285.97 ± 138.10 IU/L, P = 0.001, Table 1). The incidence of ST-segment elevation was also higher in the VF group (n = 21 [95.45%] vs n = 172 [62.8], P = 0.001, Table 1). Among the 52 patients with J wave (13 in the VF group and 39 in the non-VF group) who received elicit PCIs, J wave persisted in 13 (100%) patients of the VF group and in 32 (82.0%) patients of the non-VF group during hospital stay. Lastly, the prevalence of VF was significantly higher in patients with J wave
A
B
C
D
Fig. 1. Baseline ECGs in AMI patients. (A) and (B) show notched elevations (arrows) in inferior (A) and lateral (B) leads in the patients who had an event of VF, whereas (C) and (D). show no J wave in inferior (C) or lateral (D) leads in the patients who showed no VF during AMI.
http://dx.doi.org/10.3346/jkms.2014.29.5.685
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Kim S-H, et al. • Relationship between J Wave and Ventricular Fibrillation Table 2. ECG and laboratory findings of patients between the VF group and the Non-VF group ECG/laboratory finding Presence of notched J wave, No. (%) Presence of slurred J wave, No. (%) Heart rate beat/min QTc interval, ms K, mEq/L Mg, mg/dL
Total (n = 296)
VF group (n = 22)
Non-VF group (n = 274)
P value
41 (13.9) 11 (3.7) 73.98 ± 18.77 442.58 ± 33.63 4.07 ± 0.54 2.25 ± 0.22
12 (54.5) 1 (4.5) 76.52 ± 19.92 443.59 ± 30.64 3.93 ± 0.65 2.24 ± 0.25
29 (10.6) 10 (3.6) 73.38 ± 18.71 442.49 ± 33.91 4.08 ± 0.53 2.25 ± 0.21
< 0.001 0.999 0.52 0.883 0.208 0.793
Presence of notched J wave Absence of J wave 100 P < 0.001
Patients population (%)
80
60
40
20
29/274 (10.6%)
12/22 (54.5%)
Table 3. Multivariate logistic regression analysis of variables known as risk factors of VF Variables
Odds Ratio (95% Confidence interval)
P value
Age Male sex Hypertension Diabetes Mellitus Smoking Time from the Symptom onset to ER QTc interval Peak CK level ST-segment elevation Presence of notched J wave
0.985 (0.943-1.028) 0.289 (0.068-1.219) 0.825 (0.279-2.442) 0.254 (0.048-1.352) 0.536 (0.146-1.965) 0.999 (0.000-1.000) 1.009 (0.988-1.030) 1.000 (0.997-1.003) 15.250 (1.571-148.053) 16.547 (4.973-55.064)
0.482 0.091 0.728 0.108 0.347 0.215 0.394 0.777 0.019
http://dx.doi.org/10.3346/jkms.2014.29.5.685 • J Korean Med Sci 2014; 29: 685-690
The Relationship Between J Wave on the Surface Electrocardiography and Ventricular Fibrillation during Acute Myocardial Infarction Soo-Han Kim, Dae-Hyeok Kim, Sang-Don Park, Yong-Soo Baek, Seong-Ill Woo, Sung-Hee Shin, Jun Kwan, and Keum-Soo Park Department of Internal Medicine, Inha University Hospital, Incheon, Korea Received: 4 September 2013 Accepted: 20 March 2014 Address for Correspondence: Dae-Hyeok Kim, MD Department of Internal Medicine, Inha University Hospital, 27 Inhang-ro, Jung-gu, Incheon 400-711, Korea Tel: +82.32-890-2440, Fax: +82.32-890-2447 E-mail: [email protected]
We investigated whether the presence of J wave on the surface electrocardiography (sECG) could be a potential risk factor for ventricular fibrillation (VF) during acute myocardial infarction (AMI). We performed a retrospective study of 317 patients diagnosed with AMI in a single center from 2009 to 2012. Among the enrolled 296 patients, 22 (13.5%) patients were selected as a VF group. The J wave on the sECG was defined as a J point elevation manifested through QRS notching or slurring at least 1 mm above the baseline in at least two leads. We found that the incidence of J wave on the sECG was significantly higher in the VF group. We also confirmed that several conventional risk factors of VF were significantly related to VF during AMI; time delays from the onset of chest pain, blood concentrations of creatine phosphokinase and incidence of ST-segment elevation. Multiple logistic regression analysis demonstrated that the presence of J wave and the presence of a ST-segment elevation were independent predictors of VF during AMI. This study demonstrated that the presence of J wave on the sECG is significantly related to VF during AMI. Keywords: J Wave; Ventricular Fibrillation; Acute Myocardial Infarction
INTRODUCTION
MATERIALS AND METHODS
Primary ventricular fibrillation (PVF) during acute myocardial infarction (AMI) refers to VF that occurs early (usually < 48 hr post myocardial infarction), and is not associated with recurrent ischemia or heart failure (1). The incidence of VF was reported to be more than 10% during AMI, and VF usually occurs in a few hours after the onset of chest pain (1). VF is the most frequent cause of death in association with AMI because it usually occurs before medical contact (1). Recent studies have demonstrated that J wave on the sECG has been associated with idiopathic VF in patients who do not have structural heart disease (2). A recent study also reported that the presence of J wave is associated with ventricular arrhythmia in patients who have chronic coronary artery disease (3). So far, few studies reported that the presence of J wave in sECG is associated with VF during AMI (1, 4-6). Several variables, including J wave, were reported as significant predictors of VF, but failed to get statistical significance. Through this study, we planned to evaluate that the presence of J wave on the sECG could be a potential risk factor for VF during AMI.
Patient selection and data collection We performed a retrospective study of 317 patients diagnosed with AMI in a single center from 2009 to 2012. Among the involved 317 patients, especially in the VF group, 21 patients who did not have a sECG before AMI were excluded in this group. As a result, 22 patients were selected as the VF group and 296 patients were enrolled for data analysis. Finally, all patients were classified as having a VF or not (VF group: n = 22 [13.5%], the non-VF group : n = 274 [86.5%]). Furthermore, all patients selected for this study received coronary angiography and underwent percutaneous coronary interventions (PCIs). We perform ed a subgroup analysis according to the location of the infarction, and the infarct-related artery (IRA) were left anterior descending (LAD) artery (45.4%), left circumflex (LCX) artery (6.1%), right coronary artery (RCA) (48.5%), diagonal branch (0.3%) and left main artery (1.0%), respectively. We also checked a pre-PCI Thrombolysis In Myocardial Infarction (TIMI) flow grade before the coronary intervention.
© 2014 The Korean Academy of Medical Sciences. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
pISSN 1011-8934 eISSN 1598-6357
Kim S-H, et al. • Relationship between J Wave and Ventricular Fibrillation ECG analysis The latest ECG before AMI was reviewed for J wave characteristics. Twelve-lead ECGs were digitally downloaded from the GE Marquette MUSE system (GE Medical Systems, Milwaukee, WI, USA) and were also analyzed digitally (Adobe Acrobat X Professional; Adobe Systems Incorporated, San Jose, CA, USA). Three investigators performed ECG analysis separately and randomly to confirm correct J wave patterns. The early repolarization on the sECG was defined as J point elevations manifested through QRS notching or slurring for at least 1 mm (0.1 mV) above the baseline in at least two consecutive inferior or lateral leads. As defined through prior studies, QRS notching in ECG was defined as a positive deflection at the terminal portion of a positive QRS complex. QRS slurring in ECG was defined as a smooth transition from the QRS complex to the ST segment with upright concavity. We excluded ECGs of Brugada pattern which have J wave in anterior precordial leads (V1-V3). We measured the amplitude of J wave at the peak of the positive deflection in case of notched pattern and at the QRS-ST junction in slurred pattern. Statistics Statistical analyses were performed with SPSS statistical software (version 12.K; SPSS, Inc., Chicago, IL, USA). Continuous variables were expressed as mean ± SD and were compared by t tests. Categorical variables were expressed as percentages and
were compared by chi-square statistics or Fisher’s exact test as indicated. A multiple logistic regression analysis was used to identify the subset of variables as predictors of VF during AMI. Analyses were considered significant at a P value < 0.05 (2-tailed). Ethics statement The study protocol was reviewed and approved by the institutional review board of Inha University Hospital (Protocol No. 12-103). Informed consents were waived by the institutional review board (IRB).
RESULTS Demographic and clinical characteristics of all AMI patients Table 1 shows baseline characteristics of the study population. Among the total 22 patients of the VF group, 16 patients were males and 6 patients were females. The mean age of the VF group was a 59.95 ± 12.94 yr. The non-VF group consisted of 274 patients and male was also predominant in numbers which were 207. The mean age of the non-VF group was 61.33 ± 13.47 and was not statistically different from that of the VF group (P = 0.644). VF occurred before ER arrival in 9 patients, during ER stay before PCI in 5 patients, during PCI in 1 patient, and within 48 hr after PCI in 7 patients. In this study, we excluded patients with VF after 48 hr from the onset of chest pain. The mean time gap
Table 1. Baseline characteristics of patients between the VF group and the non-VF group Parameters
Total (n = 296)
VF group (n = 22)
Non-VF group (n = 274)
P value
Age (yr) Gender (female/male) Cardiac risk factor, No. (%) Smoking Diabetes mellitus Hypertension LDL(mg/dL) Infarct-related artery, No. (%) LAD LCX RCA Diagonal Left main trunk Pre-PCI TIMI 0, No. (%) Coronary artery disease, No. (%) One vessel disease Two vessel disease Three vessel disease Normal vessel Echocardiography LVEF LA diameter Time delay from the onset of chest pain (min) Peak CK level, IU/L ST-segment elevation, No. (%)
61.23 ± 13.41 73/223
59.95 ± 12.94 6/16
61.33 ± 13.47 67/207
0.644 0.798
176 (59.5) 64 (21.6) 155 (52.4) 117.25 ± 34.76
14 (63.6) 2 (9.1) 9 (40.9) 112.30 ± 30.29
162 (59.1) 62 (22.6) 146 (53.3) 117.64 ± 35.11
0.43 0.107 0.185 0.509 0.462
133 (45.4) 47 (6.1) 111 (48.5) 1 (0.3) 3 (1.0) 168 (57.1)
13 (61.9) 1 (4.8) 7 (33.3) 0 (0) 0 (0) 14 (66.7)
120 (43.8) 46 (16.8) 104 (37.9) 1 (0.4) 3 (1.1) 154 (56.4)
148 (50.3) 81 (27.6) 63 (21.4) 2 (0.7)
13 (61.9) 4 (19.0) 3 (14.3) 1 (4.8)
135 (49.5) 77 (28.2) 60 (21.9) 1 (0.4)
46.57 ± 8.48 39.00 ± 5.44 717.6 ± 1759.2 2,654.87 ± 4103 193 (65.2)
49.71 ± 8.37 37.33 ± 4.52 634.6 ± 135.3 12,429.78 ± 2650 21 (95.5)
46.32 ± 8.45 39.14 ± 5.49 1,815.6 ± 109.8 2,285.97 ± 138 172 (62.8)
0.493 0.064
0.078 0.144 0.007 0.001 0.001
LDL, low density lipoprotein; LAD, left anterior descending artery; LCX, left circumflex artery; RCA, right coronary artery; PCI, percutaneous coronary intervention; TIMI, thrombolysis in myocardial infarction; LVEF, left ventricular ejection fraction; CK, creatine phosphokinase.
686 http://jkms.org
http://dx.doi.org/10.3346/jkms.2014.29.5.685
Kim S-H, et al. • Relationship between J Wave and Ventricular Fibrillation from acquisition of the latest ECGs to occurrence of VF was 266 days in the VF group. In this group, the distributions of time gap were over 1 yr in 5 patients, between 1 month and 1 yr in 13 patients, and within 1 month in 4 patients. There was no statistical difference in the locations of IRA, or TIMI flow before PCI between the two groups. Also, there was no statistical difference in the numbers of stenosed coronary arteries and echocardiographic parameters, including ejection fractions of left ventricle and diameters of left atrium. Cardiac deaths were noted both in the VF group (n = 1, 4.5%) vs in the non-VF group (n = 1, 0.4%), which were not different statistically (P = 0.150). Fig. 1 shows baseline ECGs in AMI patients. Fig. 1A and Fig. 1B show notched J wave (arrows) in inferior (Fig. 1A) and lateral (Fig. 1B) leads in patients who had an event of VF, whereas Fig. 1C and D show no J wave in inferior (Fig. 1C) or lateral (Fig. 1D) leads in patients who showed no VF during AMI.
Predictors of VF during AMI We found that several conventional risk factors of VF were significantly related to VF during AMI; a time delay from the onset of chest pain to the arrival to emergency room (ER) was significantly shorter in the VF group (634.6 ± 135.3 min vs 1,815.6 ± 109.8 min; P = 0.001, Table 1). Patients in the VF group had a larger IRA, in other words, a greater cardiac enzyme level. Hence, blood concentration of creatine phosphokinase (CK) was significantly higher in the VF group (12,429.78 ± 2,650 IU/L vs 2,285.97 ± 138.10 IU/L, P = 0.001, Table 1). The incidence of ST-segment elevation was also higher in the VF group (n = 21 [95.45%] vs n = 172 [62.8], P = 0.001, Table 1). Among the 52 patients with J wave (13 in the VF group and 39 in the non-VF group) who received elicit PCIs, J wave persisted in 13 (100%) patients of the VF group and in 32 (82.0%) patients of the non-VF group during hospital stay. Lastly, the prevalence of VF was significantly higher in patients with J wave
A
B
C
D
Fig. 1. Baseline ECGs in AMI patients. (A) and (B) show notched elevations (arrows) in inferior (A) and lateral (B) leads in the patients who had an event of VF, whereas (C) and (D). show no J wave in inferior (C) or lateral (D) leads in the patients who showed no VF during AMI.
http://dx.doi.org/10.3346/jkms.2014.29.5.685
http://jkms.org 687
Kim S-H, et al. • Relationship between J Wave and Ventricular Fibrillation Table 2. ECG and laboratory findings of patients between the VF group and the Non-VF group ECG/laboratory finding Presence of notched J wave, No. (%) Presence of slurred J wave, No. (%) Heart rate beat/min QTc interval, ms K, mEq/L Mg, mg/dL
Total (n = 296)
VF group (n = 22)
Non-VF group (n = 274)
P value
41 (13.9) 11 (3.7) 73.98 ± 18.77 442.58 ± 33.63 4.07 ± 0.54 2.25 ± 0.22
12 (54.5) 1 (4.5) 76.52 ± 19.92 443.59 ± 30.64 3.93 ± 0.65 2.24 ± 0.25
29 (10.6) 10 (3.6) 73.38 ± 18.71 442.49 ± 33.91 4.08 ± 0.53 2.25 ± 0.21
< 0.001 0.999 0.52 0.883 0.208 0.793
Presence of notched J wave Absence of J wave 100 P < 0.001
Patients population (%)
80
60
40
20
29/274 (10.6%)
12/22 (54.5%)
Table 3. Multivariate logistic regression analysis of variables known as risk factors of VF Variables
Odds Ratio (95% Confidence interval)
P value
Age Male sex Hypertension Diabetes Mellitus Smoking Time from the Symptom onset to ER QTc interval Peak CK level ST-segment elevation Presence of notched J wave
0.985 (0.943-1.028) 0.289 (0.068-1.219) 0.825 (0.279-2.442) 0.254 (0.048-1.352) 0.536 (0.146-1.965) 0.999 (0.000-1.000) 1.009 (0.988-1.030) 1.000 (0.997-1.003) 15.250 (1.571-148.053) 16.547 (4.973-55.064)
0.482 0.091 0.728 0.108 0.347 0.215 0.394 0.777 0.019
